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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since free radical-mediated injury is dependent on the reintroduction of oxygen into ischemic tissues, restriction of oxygen content in the initial reperfusate has therapeutic potential. The degree to which oxygen must be restricted is crucial since hypoxic injury would continue if reperfusion O2 delivery remained below the ischemic threshold of the tissue. We examined this treatment strategy in 20 pump-perfused intestinal preparations subjected to 30 min of flow interruption. The oxygen content of the reperfusate was varied by utilizing arterial (A) or venous (V) blood; as a further modification, we also performed experiments in which hemodiluted arterial blood (HD) was the reperfusate at normal (NHD) and high (HHD) flow rates. The flow rates and O2 contents of the reperfusates were adjusted to produce either high (approximately 12 ml O2/min/100 g) or low (approximately 8 ml O2/min/100 g) levels of O2 delivery. Histologic sections, obtained after ischemia and after 1 hr of reperfusion, were blindly evaluated for mucosal injury (1 = normal to 5 = severe injury). Immediately after 30 min of ischemia, all groups had comparable histologic grades (A 2.0 +/- 0.3, V 1.8 +/- 0.3, NHD 1.6 +/- 0.3, HHD 2.3 +/- 0.3). One hour after reperfusion, intestines reperfused with blood with high O2 content and hence high O2 delivery showed significantly more damage (P < 0.001) than those with exposed to low O2 delivery during reperfusion: A 3.9 +/- 0.5 and HHD 4.4 +/- 0.4 versus V 2.7 +/- 0.5 and NHD 2.9 +/- 0.3.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Limiting oxygen delivery attenuates intestinal reperfusion injury. 143 99

The benefit of perfusion washout in both experimental and clinical skin flaps has long been debated. By perfusing ischemic rat pedicled flaps with UW solution, a recently developed, high-molecular-weight, organ-preservation medium, a 170 percent increase in the critical ischemia time of treated versus untreated control flaps was demonstrated. Sixty rats were used in this study. A 3- x 6-cm unilateral abdominal skin flap based on the superficial inferior epigastric artery and vein was raised. The flaps were divided into three groups: Group 1 (control--no perfusion washout (n = 15); Group 2 (LR)--perfusion washout with lactated Ringer's solution (n = 15); Group 3 (UW)--perfusion washout with UW solution (n = 30). Flaps were subjected to varying periods of ischemia, ranging between 8 and 30 hr. The primary ischemia time at which 50 percent of the flaps survived clinically was 10 hr for Group 1, 15 hr for Group 2, and 27 hr for Group 3. The differences between the survival rates for flaps in Groups 1, 2, and 3 were statistically significant (p less than .0005). By bathing the vascular and parenchymal cells in an impermeant preservation solution, it was hypothesized that cellular swelling would be inhibited, thereby significantly improving a skin flap's tolerance to warm ischemia. Furthermore, after reviewing the pertinent literature, it is evident that the primary critical ischemia time of 27 hr is the highest reported to date for the normothermic experimental rat pedicled flap. Clinical application of these findings, as well as the need for further studies, are discussed.
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PMID:The use of a new perfusate in experimental microvascular flaps: a threefold increase in ischemic tolerance. 175 71

A 3-year-old child with minimal change nephrotic syndrome (MCNS) developed an acute hypertensive encephalopathy characterized by coma, focal seizures, right hemiparesis, global aphasia and cortical blindness. Episodic hypertension and seizures persisted for 24 h despite intervention with antihypertensive and anticonvulsant therapy. Clinical suspicion of cortical blindness was confirmed by visual-evoked potential studies. CT scans performed 14 and 21 days after the acute episode demonstrated symmetric occipital white matter lucencies compatible with ischemia and/or associated edema. Hypertensive encephalopathy with cortical blindness and symmetric white matter hypodense lesions visualized on CT scan have recently also been described in eclampsia of pregnancy. This report documents an unusual acute hypertensive encephalopathy in childhood MCNS, unassociated with membranoproliferative glomerulonephritis, or progressive focal glomerulosclerosis.
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PMID:Acute hypertensive encephalopathy in minimal change nephrotic syndrome. 225 60

Survival of V-79 Chinese hamster cells was assessed by colony growth assay after hypothermic exposure in the presence of iron chelators. At 5 degrees C, maximum protection from hypothermic damage was achieved with a 50 microM concentration of the intracellular ferric iron chelator Desferal. A 3-hr prehypothermic incubation with 50 microM Desferal followed by replacement with chelator-free medium at 5 degrees C also provided some protection. This was not observed when the extracellular chelator DETA-PAC (50 microM) was used prior to cold storage. Treating 5 degrees C-stored cells with Desferal just prior to rewarming was ineffective, but treating cells with Desferal during hypothermia exposure after a significant period of unprotected cold exposure ultimately increased the surviving fraction. Submaximal protection during hypothermia was achieved to various degrees with extracellular chelators at 5 degrees C, including 50 microM DETAPAC and 110 microM EDTA. EGTA (110 microM) had little effect. The sensitization of cells at 5 degrees C with 200 microM FeCl3 could be reduced or eliminated with Desferal in accordance with a 1:1 binding ratio. At 10 degrees C, 50 microM Desferal, 50 microM DETAPAC, and 110 microM EDTA were as or less effective in protecting cells than at 5 degrees C. An Arrhenius plot of cell inactivation rates shows a break at 7-8 degrees C, corresponding to maximum survival for control cells and cells in 50 microM Desferal; however, the amount of protection offered by the chelator increases with decreasing temperature below about 19 degrees C, and sensitization increases above that point. It has not previously been shown that iron chelators protect against cellular hypothermia damage which is uncomplicated by previous or simultaneous ischemia. This may be relevant to the low-temperature storage of transplant organs, in which iron of intracellular origin and in the perfusate may be active and damaging.
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PMID:Factors influencing survival of mammalian cells exposed to hypothermia. IV. Effects of iron chelation. 239 29

A 3-month-old infant with anomalous origin of the left main coronary artery (LMCA) from the pulmonary trunk was evaluated using resting thallium imaging. The imaging findings were consistent with myocardial scar and ischemia of the anterolateral and posterolateral walls in the distribution of the LMCA.
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PMID:Thallium-201 imaging in anomalous left coronary artery originating from pulmonary trunk. 276 31

A 3-methyl substituted radioiodinated long chain fatty acid analogue was evaluated as an agent for the noninvasive detection of altered fatty acid uptake in reperfused, postischemic myocardium. This iodinated fatty acid analogue, 15-(para-iodophenyl)-3-methyl pentadecanoic acid, was given intravenously at 3 hours of reperfusion following 15 minutes (Group 1, n = 5 dogs) or 60 minutes (Group 2, n = 5 dogs) of left anterior descending coronary artery occlusion. Myocardial blood flow (MBF) was measured during occlusion and reperfusion with radiolabeled microspheres administered via the left atrium. Paired ultrasonic subendocardial crystals were placed in the ischemic perfusion bed to assess regional left ventricular systolic function at baseline, during ischemia and reperfusion. Electron microscopic analysis and staining with triphenyltetrazolium chloride (TTC) was performed. Groups 1 and 2 dogs had similar (p = NS) myocardial blood flows during occlusion. TTC positive 1 g endocardial segments from Group 1 (n = 98) and Group 2 (n = 71) had 37% greater fatty acid analogue activity (0.26 +/- 0.04 vs. 0.19 +/- 0.09 percent injected dose per gram; p less than 0.05) compared with TTC negative segments from Group 2 dogs (n = 37). When fatty acid analogue activity was related to near simultaneous reperfusion blood flow, this ratio was 27% greater (p less than 0.05) in TTC positive segments (0.38 +/- 0.1) compared with TTC negative (0.30 +/- 0.16) segments, and 9% greater than normal (0.35 +/- 0.09; p less than 0.05). While ischemic regions from both Groups 1 and 2 dogs became similarly dyskinetic during occlusion (systolic shortening, -11 +/- 6 vs. -11 +/- 2%; p = NS), TTC negative segments remained akinetic (= 1 +/- 7%) at 3 hours of reperfusion while TTC positive zones had recovered partial systolic function (8 +/- 22%). Electron microscopy confirmed the presence of reversible ultrastructural changes in TTC positive regions. A 60-minute occlusion, 3-hour reperfusion model adapted for in vivo single photon emission computed tomography showed a similar excess of 123I fatty acid activity over flow when compared to perfusion (as measured with 201Tl) in the ischemic border zone of 4/4 canine myocardial infarcts. We conclude that the accumulation of this non-beta-oxidized fatty acid analogue noninvasively identifies zones of discordance between fatty acid and flow distribution that are characteristic of ischemically "stunned" but viable myocardium.
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PMID:Fatty acid analogue accumulation: a marker of myocyte viability in ischemic-reperfused myocardium. 304 74

A 3-year-old child had ischemia of the left-sided upper extremity secondary to embolic disease. Arteriography showed multiple idiopathic saccular aneurysms of the left subclavian artery. Coronary arteriograms were normal. Cerebral arteriography showed ectasia of the right common carotid artery, and abdominal aortography, aneurysms of the splenic and phrenic arteries. The patient underwent brachial artery embolectomy, proximal and distal aneurysm ligation, and placement of a carotid to axillary artery polytef bypass graft. Microscopic analysis indicated intimal proliferation, normal elastic tunica media vasorum, and no evidence of an inflammatory process. Electron microscopy showed no evidence of rickettsiae. The patient's clinical appearance was similar but not identical to that of Kawasaki disease, Takayasu's disease, or periarteritis nodosa. Workup of the patient and subsequent surgical exploration failed to demonstrate a definitive cause.
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PMID:Idiopathic multiple systemic aneurysms in a child. 663 16

A 3-year clinical experience is analyzed to define preferred surgical management and amputation rates for popliteal as well as infrapopliteal arterial injuries. Ten patients with popliteal arterial trauma were successfully managed without amputation, however, five of 11 (45%) patients with infrapopliteal arterial trauma required amputation. While essentially all popliteal arterial injuries mandate repair, recommendations for repair or ligation of isolated tibial arterial injuries are based on presence of distal ischemia, the patient's associated injuries, as well as estimated operating time for reconstruction. With injury to two or three infrapopliteal arteries, distal ischemia is usually present and arterial repair indicated, unless there has been severe crush injury, prolonged delay, or extended surgery would jeopardize the patient's life. A management protocol for patients with distal ischemia related to popliteal or infrapopliteal arterial trauma should include prompt surgical intervention, liberal use of fasciotomy, intraoperative arteriography, as well as the selective use of intraluminal shunts.
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PMID:Popliteal and infrapopliteal arterial injuries. Differential management and amputation rates. 670 27

22 patients (mean age 45.08 +/- 1.38 years) with essential hypertension stage II were entered in a placebo-controlled blind trial of cilazapril, angiotensin-converting enzyme. A complex of clinical-instrumental tests comprised dipidamol test, bicycle ergometry, 199Tl myocardial scintigraphy, echo-CG. A 3-month course of cilazapril reduced myocardial hypoperfusion in 15 patients, improved left ventricular relaxation: Anti-ischemia effect of the drug was also evident.
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PMID:[The effect of cilazapril on left ventricular function and myocardial perfusion in patients with essential hypertension (hypertensive disease) stage II]. 749 43

Preconditioning the brain with sublethal cerebral ischemia induces tolerance to subsequent lethal periods of ischemia (ischemic tolerance). The purpose of this study is to investigate the role of low-molecular weight stress proteins, 27-kDa heat shock protein (HSP27) and alpha B crystallin, in ischemic tolerance. We measured the content of these proteins with enzyme immunoassay in the rat hippocampus and cerebral cortex following 6 min of ischemia with and without preconditioning with 3 min of ischemia and 3 days of reperfusion. We also visualized the localization of HSP27 immunohistochemically in comparison with that of HSP70. A 3-min period of ischemia caused a 2.4-fold increase in HSP27 content in the hippocampus after 3 days. Immunohistochemical localization of HSP27 was found in glial cells in all subregions of the hippocampus, whereas HSP70 immunostaining was seen only in CA1 pyramidal neurons. HSP27 content in the hippocampus decreased 2 h after 6 min of ischemia. HSP27 content progressively increased in the unpreconditioned hippocampus after 1 and 3 days, but returned to preischemic levels in the preconditioned hippocampus. HSP27 and HSP70 immunostaining was seen in CA1 pyramidal neurons after 1 day both with and without preconditioning. After 3 and 7 days, an intense HSP27 staining was observed in reactive glial cells in the CA1 without preconditioning, whereas the staining decreased in the preconditioned hippocampus. HSP70 staining was seen only in neurons at these time points. We observed no significant changes in HSP27 content in the cerebral cortex although neurons in the third and fifth layers were immunostained after 1 and 3 days. We observed no alterations in alpha B crystallin content after ischemia both in the hippocampus and the cortex. The present study demonstrated that cerebral ischemia induces HSP27 expression but not alpha B crystallin. Both HSP27 and HSP70 induction had a good temporal correlation with the induction of ischemic tolerance. However, different sites of action were suggested because the localization and cell types of HSP27 induction were quite different from those of HSP70 induction. The result suggests that it is unlikely that HSP27 is directly involved in the protection afforded by ischemic preconditioning.
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PMID:Induction of 27-kDa heat shock protein following cerebral ischemia in a rat model of ischemic tolerance. 813 Oct 73


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